Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease (ESRD) in the United States and many other countries. DKD occurs through a variety of pathogenic processes that are in part driven by hyperglycemia and glomerular hypertension, leading to gradual loss of kidney function and eventually progressing to ESRD. In type 2 diabetes, chronic hyperglycemia and glomerular hyperfiltration leads to glomerular and proximal tubular dysfunction. Simultaneously, mitochondrial dysfunction occurs in the early stages of hyperglycemia and has been identified as a key event in the development of DKD. Clinical management for DKD relies primarily on blood pressure and glycemic control through the use of numerous therapeutics that slow disease progression. Because mitochondrial function is key for renal health over time, therapeutics that improve mitochondrial function could be of value in different renal diseases. Increasing evidence supports the idea that targeting aspects of mitochondrial dysfunction, such as mitochondrial biogenesis and dynamics, restores mitochondrial function and improves renal function in DKD. We will review mitochondrial function in DKD and the effects of current and experimental therapeutics on mitochondrial biogenesis and homeostasis in DKD over time.

在美国和许多其他国家，糖尿病肾病 (DKD) 是终末期肾病 (ESRD) 的主要原因。DKD 通过多种致病过程发生，这些致病过程部分由高血糖和肾小球高血压引起，导致肾功能逐渐丧失并最终发展为 ESRD。在 2 型糖尿病中，慢性高血糖和肾小球高滤过导致肾小球和近端肾小管功能障碍。同时，线粒体功能障碍发生在高血糖的早期阶段，已被确定为 DKD 发展的关键事件。DKD 的临床管理主要依赖于通过使用多种减缓疾病进展的疗法来控制血压和血糖。因为随着时间的推移，线粒体功能是肾脏健康的关键，改善线粒体功能的疗法可能对不同的肾脏疾病具有价值。越来越多的证据支持这样一种观点，即针对线粒体功能障碍的各个方面，例如线粒体生物合成和动力学，可以恢复线粒体功能并改善 DKD 患者的肾功能。我们将回顾 DKD 中的线粒体功能以及当前和实验疗法对 DKD 中线粒体生物发生和稳态随时间的影响。